DESCRIPTION (from abstract): The long-term objective of this research is to relate functional deficits in patients with visual disorders to underlying cellular pathophysiology. A better understanding of these relationships will be useful in design of treatment trials, in selecting tests for evaluation of individual patients, and in guiding biomolecular and physiological studies. The research uses quantitative models, rigorous psychophysical methods, and carefully selected patient populations to investigate the linkage between functional defects and biological damage. The proposed research focuses on psychophysical measures of ganglion cell function in relative scotomas (local regions of reduced sensitivity) in patients with progressive diseases which primarily damage only one class of neuron: retinal ganglion cells (glaucoma) or photoreceptors (retinitis pigmentosa). For both diseases, there is debate over the effects of cell damage, and over the mechanisms of cell death. There are 3 specific aims: 1 ) To model effects of ganglion cell damage on perimetric thresholds. and to apply these models to patient data. Qualitative models have been proposed to account for relative scotomas in terms of retinal ganglion cell damage, but quantitative models have not been developed. Data on human and macaque ganglion cell mosaics will be used to build a quantitative model to link ganglion cell damage with perimetric threshold elevations, and apply this to normal and patient data gathered with both standard perimetric stimuli and innovative stimuli. 2) To investigate reversibility of visual deficits caused by glaucoma. It is debated whether glaucomatous defects are reversible. Local sensitivity of discrete ganglion cell mosaics will be measured in patients with glaucoma before and after acute surgical reduction of intraocular pressure to determine if visual function improves. 3) To evaluate temporal processing in relative scotomas of patients with retinitis pigmentosa (RP). There is debate over whether temporal defects in RP are due to reduction in cone sensitivity (reduced quantal catch and/or transduction efficiency), or to a temporal processing defect in the cones or the inner retina. Temporal sensitivity will be measured in relative scotomas of patients with RP, at a mean retinal illuminance which allows cone sensitivity loss to be distinguished from purely temporal.